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19 Urinaryretention
Jalesh N. Panicker, Ranan DasGupta, Sohier Elneil and Clare J. Fowler
of the outflow tract. Urethrocystoscopy is then usuallyperformed.
Impairment of bladder emptying may manifest as com-
Mechanical causes in men generally result from an
plete or partial urinary retention, and be either acute or
anatomical obstruction to the bladder outflow, due
chronic. The conditions under which retention occur
for example to an enlarged prostate gland, urethral
are many and varied, indicating there must be many
stricture, or even a phimosis. Prolonged obstruction
different causes which effect the same end result.
(chronic retention) can eventually result in detrusor
Acute complete urinary retention is not uncommon
"failure" or hypocontractility. As a general rule it is
following surgery irrespective of the operation site and
advisable for a man with a longstanding neurological
is attributed to pain and the effects of postoperative
condition to be investigated urologically before
analgesia, with full recovery of voiding when these
ascribing new bladder symptoms to his neurological
effects wear off. Although complete retention can occur
disease: a urethral stricture may develop some years
acutely, it may be due to a high post-void residual
after prolonged catheterization during a period of
volume, of which the patient may or may not be aware.
unconsciousness or paralysis in intensive care.
Partial retention may be discovered incidentally or as a
In women, there is no specific diagnosis of bladder
result of investigation of a patient reporting the sensa-
outlet obstruction, as occurs in the men. However,
tion of incomplete voiding in association with voiding
external factors can obstruct the urethra. These
difficulty or a poor stream. When a voiding disorder
include urethral diverticulae, uterine and cervical
occurs in conjunction with detrusor overactivity, as
fibroids and vaginal wall cysts.
commonly occurs with spinal cord disease, it may beconceptually helpful to think of the high residualvolume as the result of "incomplete emptying."
Functional urinary retention with associated
Patients with retention may present to a urologist,
uro-gynecologist or neurologist.
neurological dysfunctionSpinal cord disease is a common cause of incompletebladder emptying although this usually occurs in
Causes of urinary retention
combination with detrusor overactivity so that the
The underlying causes of urinary retention may be
clinical picture is dominated by urgency incontinence.
either structural or functional (Table 19.1).
Sometimes, however, the impaired emptying may bethe more prominent part of the disorder, resultingoccasionally in complete retention. An acute spinal
Structural causes
cord injury causing "spinal shock" will result in detru-
Once a diagnosis has been made, most structural
sor areflexia lasting some weeks (Chapter 15). Be the
causes are amenable to surgical correction. Urological
spinal cord pathology causing bladder dysfunction
or gynecological assessment includes taking a history,
acute or chronic, its other neurological features will
genital and pelvic examination, and where indicated,
be readily apparent: it is extremely unusual for a
urodynamic studies and possibly specialized imaging
spinal lesion to cause bladder dysfunction without
Pelvic Organ Dysfunction in Neurological Disease: Clinical Management and Rehabilitation, ed. Clare J. Fowler,Jalesh N. Panicker & Anton Emmanuel. Published by Cambridge University Press. # Cambridge University Press 2010.
Section 3: Specific conditions
Table 19.1. Causes for urinary retention
Mechanical (anatomical)
Congenital malformations
Posterior urethral valves
Prostate and bladder
Gynaecological, e.g. leiomyomas,pregnancy, vaginal wall cysts
Urethral, e.g. urethral diverticulumor cysts
Stenosis and strictures
Urethral stricture, bladder neckstenosis
Bladder or urethral
Urogenital prolapse
Functional Neurological causes
Detrusor external sphincter dyssynergia and
Spinal cord injury or disease
poorly sustained detrusor contraction
Detrusor areflexia or hypocontractility
Multiple system atrophy
Lesion of conus medullaris orspinal roots
Pure autonomic failure
Radical pelvic surgery
Non-neurological causes
Primary failure of urethral sphincter relaxation
Fowler's syndrome (FS)
Anticholinergic drugs or thosewith anticholinergic activity
Primary detrusor myogenic failure
there being long tract signs on neurological examin-
understanding neurogenic skeletal muscle weakness,
ation. Normal lower limb-evoked potentials may be
is not directly applicable to neurogenic bladder
reassuring, as will a normal MRI of the spine, an
disorders. Whereas damage to an anterior horn cell
investigation which is frequently performed but rarely
in the cord or its motor axon in a ventral root or
reveals unsuspected abnormalities in this context.
peripheral nerve will result in denervated striated
Incomplete bladder emptying has been identified
muscle and flaccid paralysis, a sacral root lesion
as a feature that can be used to distinguish between
does not produce detrusor denervation. This is
MSA and Parkinson's disease [1] and an increasing
because the S2–S4 roots contain the preganglionic
post-micturition residual volume has been demon-
parasympathetics destined for ganglia in the pelvis
strated as disease progresses in MSA [2] (Chapter 13).
from which short postganglionic fibers originate to
Just occasionally complete urinary retention can be
innervate the detrusor smooth muscle (Chapter 1)
a presenting symptom of MSA, although on careful
(Fig. 19.1).
clinical examination other neurological features will be
So it is that subsacral cord or cauda equina lesions
(Chapters 15 and 17) produce an insensate "decen-
The neurological concept of "upper" and "lower
tralized" bladder which may exhibit poor compliance
motor neuron" lesion, which is fundamental for
or detrusor overactivity, presumably due to preserved
Chapter 19: Urinary retention
Fig. 19.1. Whereas sphincter denervation is a consequence of sacral root injury, root injury or damage to the pelvic nerves in the pelvisproduces a "decentralized" bladder since the postganglionic innervation is intact.
urothelial-detrusor reflexes and continuing intact
currently lacking. Presumably, this same condition
sympathetic innervation, rather than an acontractile
makes up a proportion of the women with unex-
detrusor and urinary retention. Retention can, how-
plained urinary retention.
ever, result from damage to the ganglia as may occurin the condition of pure autonomic failure with gan-glionic autoantibodies, or surgical damage to the gan-
Fowler's syndrome (FS)
glia and postganglionic fibers during radical pelvic
Urinary retention in young women in whom no uro-
surgery (Chapter 18). Incomplete emptying or com-
logical, gynecological or neurological abnormality
plete retention can also result from the small fiber
can be identified present a diagnostic dilemma.
involvement of diabetic or amyloid neuropathy which
Women experiencing otherwise unexplained urinary
may affect the pre- and postganglionic innervation
retention are more numerous than men and in a young
(Chapter 18).
woman a primary failure of sphincter relaxation (FS)
What may either be a neuropathy confined to
should be suspected. Previously, isolated urinary
the visceral innervation, or in infants a myopathy,
retention in young women in whom no abnormalities
can cause "visceral enteropathy." This can present as
on routine tests could be found was purported to be of
chronic idiopathic pseudo-obstruction (CIPO), a rare
psychogenic or hysterical origin [7–13], although a
syndrome characterized by gross distension of pre-
disorder of sphincter relaxation in young women has
dominantly the small bowel without any anatomical
been recognized for several years. Moore observed
or mechanical obstruction. Bladder dysfunction has
urethral sphincter hypertrophy during cystoscopy
been reported in 10–69% of patients with CIPO [3–5].
in a series of women with voiding dysfunction [14]
Urodynamic investigations reveal similar changes to
and Raz observed elevated urethral closure pressures
those seen in diabetic cystopathy including detrusor
in a group of young women with urinary retention and
hypocontractilty, increased residual volume and
postulated that their retention was due to spasticity of
decreased bladder sensation [3]. Many are able to void
the striated urethral sphincter or pelvic floor [15].
with the Valsalva maneuver or using catheters.
Fowler and colleagues then recorded myotonia-like
In men, there is an uncommon condition where
electromyographic (EMG) activity in the striated
painless urinary retention presents without a mech-
urethral sphincter of women presenting with urinary
anical cause or associated neurological disorder. They
retention [16] and proposed that the urinary retention
have neither accompanying constipation nor sexual
was due to a primary impairment of sphincter
dysfunction and extensive investigation fails to reveal
relaxation [17].
any underlying abnormality. It has been speculatively
Although the EMG activity sounds superficially
proposed that this disorder is due to some abnormal-
like myotonia, detailed analyses show that the charac-
ity of the intrinsic afferent innervation, possibly loss
teristic descending sound is due to a decelerating
of the "myofibroblast" or interstitial cells, thought to
component of a complex repetitive discharge [18]
be an integral part of the bladder stretch-sensing
(Fig. 19.2A). When a number of generators of this
mechanism [6], although any evidence for this is
type of activity are heard, the sound has been likened
Section 3: Specific conditions
Fig. 19.2. Electromyographic recording from the striated urethral sphincter of a woman in complete urinary retention. A. "Deceleratingburst." B. "Complex repetitive discharge." When heard over the audio output of the EMG machine, it is likened to the sound of helicopters.
Chapter 19: Urinary retention
to that of underwater recordings of whale song [19].
Table 19.2. Fowler's syndrome: clinical features and laboratory
Complex repetitive discharges without deceleration
produce a sound like helicopters over the audio-
amplifier of the EMG machine (Fig. 19.2B). Jitter
analysis of the components of the complex repetitive
Aged between onset of menarche and
discharges shows that this is so low that it must be due
to ephaptic transmission between muscle fibers [18]generating repetitive, circuitous self-excitation. It is
No evidence of urological,
this abnormal activity which is thought to prevent
gynecological or neurological disease
relaxation of the sphincter and cause urinary reten-
Retention with a volume in excess of
tion or voiding dysfunction [18]. Other studies have
demonstrated an association between complex repeti-
No sense of urinary urgency despite
tive discharges and increased post-void residual
high bladder volumes
urine [20] and voiding dysfunction [21].
Straining does not help emptying
At the time of the original description of FS, many
of the patients were observed to be hirsute, obese
Sense of "something gripping" or
and to have menstrual irregularities and there
difficulty on removing catheter
appeared to be a clinical association with polycystic
No history of urological abnormalities in
ovaries (PCO) [17]. This association is now no
childhood or associated abnormalities
better understood than when the observation was first
of the urinary tract
made, and although the coincidence of PCO and
Association with polycystic ovarian
retention is by no means inevitable, a hormonal
syndrome and endometriosis
basis for the EMG abnormality seems likely and it
Raised urethral pressure (>50%
has been proposed that it is the result of a hormonally
expected value for age)
dependent channelopathy [22]. The same type ofsphincter disorder has not been found in men
Increased sphincter volume (>1.8 ml on
with otherwise unexplained retention. According
to the recent work of O'Connell and colleagues
Characteristic urethral sphincter EMG
[23] the distal urethra is a constituent part of theclitoris, forming the "clitoro-urethrovaginal complex"[24] and clearly the distal urethra has major sex-
surgical procedure using regional or general anesthe-
sia. That the surgical procedure can be distantfrom the pelvis and as minor as wisdom teeth extrac-tion suggests the significant factor is the general
Clinical features and investigations
anesthetic. In some cases it is possible to elicit a
A retrospective study by Swinn et al. defined the
prior history of poor voiding with an interrupted
characteristic features of FS [25]. Patients are typically
flow with which the woman may have been uncon-
young post-menarche females who become unable to
cerned but indicating at least some pre-existing
void and present with painless urinary retention,
abnormality. Why then a transient event such as a
having a demonstrated residual volume exceeding
general anesthetic should precipitate retention which
1 l at some stage in the evolution of their disorder
does not resolve remains unknown and has undoubt-
(Table 19.2). Although they may experience pain if
edly been the cause of a number of medicolegal
bladder distension becomes extreme, they do not
report the expected urgency at such a large bladder
If a trial without a catheter fails, the woman is usually
capacity. Straining does not help emptying and intui-
introduced to clean intermittent self-catheterization
tively women feel they must promote sphincter relax-
and her loss of sensation of urgency and their large
ation to void by whatever means they can.
capacity mean she can go for long intervals with-
The women often report that there has been an
out catheterizing. However, catheterization is often
antecedent event prior to the onset of their retention,
painful, particularly on removing the catheter,
such as an obstetric, gynecological or urological
with many women complaining of a sensation of
Section 3: Specific conditions
"something gripping" as the catheter is withdrawn.The discomfort with self-catheterization appears tobe much greater for these women than is reportedby similarly aged young women with multiplesclerosis and it is not uncommon for the difficul-ties to be so extreme that a suprapubic catheter isrequired. This is clearly a thoroughly unsatisfactoryarrangement for an otherwise healthy youngwoman.
Routine cystometry demonstrates a large-capacity
bladder without the usual sensations during the fillingphase, and filling is often stopped at 500 ml ongrounds of safety although the subject's capacity ismuch greater. The patient is then unable to initiate
Fig. 19.3. UPP in woman with Fowler's syndrome.
voiding and no rise in detrusor pressure observed.
The diagnostic investigation is urethral sphincter
EMG using a concentric needle electrode (see Chap-
(SNM) and the evidence from functional brain
ter 4), to detect the abnormality previous described.
imaging suggests the underlying mechanism of the
However, despite paraurethral injection of local anes-
retention is more complicated. That contraction of
thetic first, which may itself be painful, this test is
the striated urethral sphincter can inhibit detrusor
uncomfortable and furthermore the information
contraction and suppress bladder afferents is known
obtained is qualitative rather than quantitative:
from animal experiments [29], although this has
"is there or is there not abnormal EMG activity?"
been little studied as it is a difficult phenomenon to
It provides only limited information about the
investigate in animals. We do know that in health,
severity of abnormality and expected resulting dys-
urethral afferents are hard-wired in the spinal cord to
function, and it is sometimes difficult to be sure that
suppress sensation, inhibit bladder activity and mod-
"sufficient abnormality" has been found to account
erate ascending bladder signals [30] (Chapter 1).
for a woman's complete urinary retention. The ureth-
This is the neural basis for the "pro-continence reflex"
ral pressure does however give insight into the func-
whereby voluntary contraction of the sphincter
tional abnormality. Using an infusion technique
reduces urgency, and it is enhancement of this reflex
(withdrawal of an 8 Fr urethral catheter at 2 mm/s
that is the basis for physiotherapy exercises to encour-
while infusing saline at 2 ml/min), maximum urethral
age pelvic floor contractions to control urgency
closure pressure (MUCP) can be measured (Fig. 19.3)
incontinence. Feed forward from the guarding reflex
and typically women with FS are found to have
may further activate the pro-continence reflex in
resting values in excess of 100 cm of water [26].
health, both mechanisms combining to maintain
The formula of 92 – age (in years) is used to derive the
bladder control as the bladder fills. In FS it is
expected pressure, based on the work of Edwards
hypothesized that extreme involuntary sphincter con-
and Malvern [27]. Wiseman et al. [28] also proposed
traction results in accentuation of the pro-continence
that ultrasound measurement of sphincter volume was
reflex to the point that bladder sensation is suppressed
helpful to detect the hypertrophy of the striated sphinc-
and detrusor contraction
ter resulting from sustained overactivity; but operator
Certainly an absence of sensation with gross bladder
variability in this measurement has restricted its useful-
filling is characteristic of this condition and further
ness in the diagnostic algorithm for these patients.
implies that signals from the bladder reaching thebrain are abnormally weak. The recent surprisingresults of an fMRI research study provide confirm-
Pathogenesis of retention
ation of this hypothesis [31].
Initially the findings seemed to suggest that urinary
Repeated bladder filling and emptying of only
retention in these young women was simply the result
50 ml at the baseline "bladder empty" condition
of chronic outflow obstruction owing to poor sphinc-
showed widespread negative responses to bladder
ter relaxation. However the restoration of detrusor
infusion (appearing blue in Fig. 19.4) in six women
Chapter 19: Urinary retention
Fig. 19.4. Functional MRI study in Fowler's syndrome. Responses to bladder infusion for the six women, rendered (projected) on the brain surface.Red ¼ activation; blue ¼ negative response. A. Session at baseline with a near-empty bladder. B. at baseline with a full bladder. C. After SNM anda near-empty bladder. D. After SNM and a full bladder. Positive responses (red) indicate activation by bladder infusion. Negative responses (blue)indicate that the fMRI signal is smaller during infusion than during withdrawal. For the session at baseline with an empty bladder (Fig. 19.2A),the brain responses to bladder infusion (relative to withdrawal) were almost exclusively negative. See plate section for color version.
with FS, quite different from the activations seen in
being that bladder filling in these women elicits
"normal" individuals. Negative responses indicate
abnormally strong urethral afferent signals that
that the fMRI signal is smaller during infusion than
inhibit bladder afferent activity reducing input to
during withdrawal, the interpretation of this finding
(and so deactivating) the periaqueductal gray (PAG)
Section 3: Specific conditions
Fig. 19.5. Correlation between the defect in the interoception of filling, i.e. an abnormal negative response, and the maximumurethral closure pressure (MUCP), a proxy measure of the abnormality of sphincter activity, in the individual subjects. See plate sectionfor color version.
and higher centers. Furthermore a correlation was
(and concomitant decreased residual volume) over
demonstrated between the defect in the interoception
48–72 hours [32] (Fig. 19.6).
of filling (i.e. the abnormal negative responses) and
A study by DasGupta and Fowler included assess-
the maximum urethral closure pressure, a proxy
ment of striated sphincter EMG and MUCP before
measure of the abnormality of sphincter activity,
and after SNM, and showed no overall change in
in the individual subjects (Fig. 19.5).
these parameters in women with restored voiding
Our understanding of the mechanism of action
[33]. Urodynamic data from that study showed that
of SNM in FS has developed through a number of
the restoration of voiding is not due to changes in
experimental approaches including urodynamics,
sphincter overactivity but an improvement in detru-
electrophysiological, brain imaging and clinical obser-
sor contractility: a surrogate measurement of "work
vation. An elegant demonstration of the restoration of
done" by the detrusor suggested that the restored
sensation and its timing in relation to the start of
voiding was achieved by overcoming obstructed
neuromodulation was described by Swinn et al.
bladder outflow.
Within hours of switching on the stimulator for
A PET study suggested SNM probably restored
SNM, bladder sensations return and the woman is
voiding in women with FS by resetting brainstem
able to void again. In a study that measured the
function [34]. What was demonstrated with PET
voided volumes and the post-micturition residual
imaging was that with SNM afferent activity reached
volumes before and after the onset of neuromodula-
the midbrain [34], and more recently with functional
tion, there continued to be increased volumes voided
magnetic resonance imaging (fMRI) [31] it reached
Chapter 19: Urinary retention
Volume of urinepassed (ml)
Catheter vol.Time (hours relative to PNE insertion)
Fig. 19.6. Within hours of switching on the stimulator for sacral neuromodulation (SNM) bladder sensations return and the womanis able to void again. A study that measured the voided volumes and the post-micturition residual volumes before and after the onset ofneuromodulation showed that there continued to be increased volumes voided (and concomitant decrease in residual volume) over48–72 hours. From [32], with permission.
the PAG (Fig. 19.7). It is therefore hypothesized
studies have demonstrated significant urodynamic
that SNM blocks the urethral inhibition of afferent
findings in patients receiving intrathecal and intra-
information flow from the bladder, thus re-enabling
venous opiates, including impaired bladder sensation,
detrusor hypocontractility and increased bladder cap-acity with normal urethral pressures [36, 37].The effect may be dose-related as evidenced by the
Opiates and voiding dysfunction
increased risk of postoperative retention with patient-
Although the theory outlined above provides the
controlled analgesia as compared to intramuscular
main basis for understanding urinary retention in
opioids [38]. Tramadol in particular has been
young women with FS, the role of medication in
shown to have a potent effect in reducing detrusor
causing retention, opiates in particular, has recently
overactivity in experimental animal models [39, 40].
become the focus of attention. Drugs with anticholi-
The Netherlands Pharmacovigilance Foundation
nergic activity (e.g. antipsychotic drugs, antidepres-
reported five cases where there was a temporal asso-
sant agents and anticholinergic respiratory agents),
ciation between transient voiding dysfunction or
urinary retention with the use of tramadol [41].
steroidal anti-inflammatory drugs (NSAIDs) and cal-
Animal studies suggest that the activation of µ
cium channel antagonists [35] are well known to
opioid receptors in the PAG region of the midbrain
affect voiding but we have recently become increas-
inhibit detrusor contractions, thus resulting in urin-
ingly aware of the effect of opiates in causing a failure
ary retention [42]. Both men and women taking
to void. Although notorious as a potent cause of
these medications are similar to women with FS
constipation, the role of opiates as a cause of urinary
in that they lack sensations of urgency but by
retention seems to be less well recognized. Previous
contrast they can usually empty to completion.
Section 3: Specific conditions
Fig. 19.7. PET imaging showed that with SNM afferent activity reached the midbrain [34] and more recently with functional magnetic resonanceimaging (fMRI) [31] the PAG and right insula showed activation. Reproduced with permission. See plate section for color version.
The effect of these medications on a patient with
have neurological or urological disease, some of
"incomplete" FS is not clear but it may well be syner-
whom have personality traits which many medical
gistic and precipitate complete retention. In a
practitioners regard as "manipulative or immature."
prospective study of 61 referrals to our department
This has led to the observation that "Fowler's
for investigation and management of urinary reten-
syndrome does not keep good company." In retro-
tion, the cause could be identified in only 19. How-
spect women taking high doses of opiates almost
ever, 24 of the 61 patients were using significant doses
certainly comprised a cohort of such cases and
of opiates and in 34 of them, no other cause for
the possibility that the effect of opiates is to accentu-
urinary retention could be identified [43] (Fig. 19.8).
ate the pathophysiological consequences of an over-
This recent observation explains a longstanding diffi-
active sphincter may explain why 29% of those
culty for the originator of FS which has been the
diagnosed with FS on the basis of abnormal sphincter
defence of the proposal that there is an organic cause
EMG and an elevated MUCP were also taking opi-
for urinary retention in young women who do not
ates [43] (Fig. 19.8).
Chapter 19: Urinary retention
Fig. 19.8. Opiate use in a prospective study of women presenting with urinary retention (n ¼ 61) [43].
Recently, Elneil et al. performed a retrospective
et al. showing 76.2% efficacy at 70.5 months [45]
analysis of the outcome of "two-stage" sacral neuro-
and Elhilali et al. showing efficacy of 78% at 77
modulation in treating 100 women with chronic urin-
months [46]. Importantly, De Ridder and colleagues
ary retention, 25 of whom were on opiate medications
showed that women with urinary retention due to FS
prescribed by their general practitioners or pain phys-
had a better outcome from SNM at five years than
icians for symptomatic management of chronic back,
those without an abnormal sphincter EMG (72% vs.
pelvic or abdominal pain. Eight of these women had
46%) [47]. Our results were similar, with 78% versus
been diagnosed with FS on the basis of their history, a
43% efficacy, respectively [44].
raised UPP and abnormal sphincter EMG and a fur-
Having changed to the "two-stage" procedure (see
ther eight had a suitable history and raised UPP but
Chapter 7) in 2004, a recent, medium-term follow-up
had not had a sphincter EMG test.
of 100 women showed that the efficacy of the first
It is now being hypothesized that FS results in
stage of the implant was 81% and an abnormal
excessive levels of endogenous encephalins, possibly
sphincter EMG was a predictor for responsiveness
at the level of the sacral spinal cord [43], and that in
[48]. Stage 2 was carried out in 77 patients and com-
some patients this may be compounded by the effect
plete voiding was restored in 54 patients, improved
of exogenous opiates. Sacral neuromodulation, but
bladder emptying in 9 patients but failure in 14
not pudendal nerve stimulation, somehow success-
patients. Of the 77 women, only 49 had had sphincter
fully counteracts that pathological condition.
EMG but all had had UPP measurement. An elevatedUPP was found to predict a good response to stage 2but the EMG findings were inadequately powered
to demonstrate an effect. A new surgical interven-
In the analysis of our initial cohort of 60 women who
tion was required in 40 patients either because of leg
underwent percutaneous nerve evaluation (PNE) and
pain or pain in relation to the battery site, lead dis-
subsequent implant, when followed up with a mean
placement or fracture, loss of efficacy or battery site
interval of 7 years, 70% were voiding spontaneously
[44]. This is in keeping with the findings from other
As mentioned above, 25% of this cohort was being
centers of the longer-term efficacy of SNM as a treat-
treated with opiates but the use of opiates was shown
ment for non-obstructive retention, van Voskuilen
to have no effect on the outcome of stage 1 or stage
Section 3: Specific conditions
2, nor was it a determining factor for the need for
access to the internet, more patients and their relatives
revision surgery. A deduction that can be made from
are becoming aware that SNM is an intervention that
the observation that those taking and those not taking
can restore voiding for some and they naturally seek
opiates had a comparable response to SNM suggests
out the opportunity to be treated by this intervention.
that its mechanism of action is likely to involve an
The result is that both women and men with chronic
anti-inhibitory effect of neurotransmitters common
retention are being referred to centers that offer this
in both groups, possibly at opiate receptors in the
treatment, although only a small proportion may be
cord or PAG. Recently Chen et al. [49] have demon-
strated that the inhibitory effect of pudendal nerve
That SNM restores voiding in FS is well estab-
stimulation on bladder reflexes in experimental cats
lished [32], its long-term efficacy has been shown to
can be influenced by naloxone, suggesting an inhibi-
be greatest in women with FS [47], and furthermore
tory role of endogenous opioids as a mediator for the
we now have a scientific basis for understanding how
stimulation effect. However, pudendal nerve stimula-
it works in this condition [31, 34]. The efficacy of SNM
tion at standard frequencies has been found not to be
in other causes of retention (most of which are of
effective in restoring voiding in women with retention
unknown cause) is much less certain [52]. This pre-
(personal communication, Dr. Spinelli), suggesting
sents a problem when counseling patients, although
that pudendal nerve stimulation and sacral neuromo-
many centres operate a policy that it is reasonable to
dulation produce a fundamentally different effect on
carry out a PNE, or nowadays more likely stage 1 with
the neural control of micturition. It is postulated that
tined lead, to test for efficacy in each individual wish-
SNM may specifically counteract an excessive level of
ing to be considered for long-term SNM. Certainly the
endogenous, and sometimes additional exogenous,
indications for SNM seem to be widening and its effect
in men with non-surgical urinary retention deservesfurther investigation.
Management of chronic urinaryretention and SNM
Selection of patients with retention for SNM
The alternatives for management of chronic urinary
It is assumed that patients have had structural or
retention in women are limited. Many patients are
neurological diagnosis excluded or at least uncovered.
treated with a-blockers, urethral dilatation or ureth-
Although a diagnosis of FS is now established as a
rotomy with little long-term success. Working on the
predictor for a good outcome for SNM [32, 47, 48],
principle that a phosphodiesterase inhibitor might
sphincter needle EMG is not an easy test for the
increase nitric oxide availability in the sphincter and
patient or electromyographer and the test is not
thus improve sphincter relaxation, we treated five
widely performed outside academic centers. However,
women with FS in a placebo-controlled trial with
urethral pressure profile is a standard urodynamic
sildenafil but unfortunately without benefit [50].
investigation and it is recommended that this is more
Although an early study of the effect of injection of
widely used in the preoperative assessment of women
botulinum toxin into the striated urethral sphincter
with retention. It will be elevated in women with a
[51] failed to restore voiding in women with FS, there
primary disorder of sphincter relaxation (i.e. FS) but
is some evidence that this is an intervention worth
abnormally low in women who have urinary retention
as a result of a damage to innervation of the sphincter
Whilst no pharmacological has yet been dis-
and detrusor. Consideration of patients taking opi-
covered to be effective, many women face the pro-
ates, which may either be the cause alone or a contrib-
spect of indefinite, often uncomfortable intermittent
uting factor to urinary retention [43], is a difficulty.
catheterization or a permanent drainage procedure
Clearly if the dosage is such that the medication
(either an indwelling catheter or a surgical urinary
appears to affecting daily function or addictive behav-
diversion procedure). This is an unsatisfactory solution
iour patterns are evident, then steps to stop or reduce
for young women and their problem is commonly
it, although difficult to achieve, would seem to be a
compounded by a deep dissatisfaction because they
better medical approach than SNM.
may have had no explanation as to why they continue
Since SNM it is a resource-intensive proce-
to have chronic urinary retention. With increasing
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Fig. 19.4. Functional MRI study in Fowler's syndrome. Responses to bladder infusion for the six women, rendered (projected) on the brainsurface. Red ¼ activation; blue ¼ negative response. A. Session at baseline with a near-empty bladder. B. at baseline with a full bladder. C. AfterSNM and a near-empty bladder. D. After SNM and a full bladder. Positive responses (red) indicate activation by bladder infusion. Negativeresponses (blue) indicate that the fMRI signal is smaller during infusion than during withdrawal. For the session at baseline with an emptybladder (Fig. 19.2A), the brain responses to bladder infusion (relative to withdrawal) were almost exclusively negative.
Fig. 19.5. Correlation between the defect in the interoception of filling, i.e. an abnormal negative response, and the maximum urethralclosure pressure (MUCP), a proxy measure of the abnormality of sphincter activity, in the individual subjects.
Fig. 19.7. PET imaging showed that with SNM afferent activity reached the midbrain [34] and more recently with functional magneticresonance imaging (fMRI) [31] the PAG and right insula showed activation. Reproduced with permission.